An examination of the salvage of circulating pyrimidines by mouse tissues was completed. Regulation of de novo and salvage mechanisms for pyrimidine biosynthesis in wild type human breast carcinoma cells was compared with cells that overproduce enzymes of the de novo pathway by gene amplification. Efforts to block pyrimidine salvage in vivo were continued. Several new compounds to block uridine transport and/or phosphorylation were designed, synthesized, and evaluated. A preparation of uridine phosphorylase, purified from an overproducing mutant of E. coli, was studied for its effects on circulating uridine concentrations and is currently undergoing evaluation as a chemotherapeutic agent. Efforts to manipulate the hepatic output of purines and pyrimidines were continued. An analog of methylthioadenosine was synthesized to evaluate the role of MTA phosphorylase in the hepatic regulation of circulating adenine.